Increased b2-Adrenergic Receptor Activity by ThyroidHormone Possibly Leads to Differentiation andMaturation of Astrocytes in Culture
2007
Our earlier studies indicate a downsteam regulatory role of the badrenergic
receptor (b-AR) system in thyroid hormone induced differentiation and
maturation of astrocytes. In the present study we have investigated the contributions of
the subtypes of b-AR in the above phenomenon. (2) Primary astrocyte cultures were
grown under thyroid hormone deficient as well as under euthyroid conditions.
[125I]Pindolol ([125I]PIN) binding studies showed a gradual increase in the specific
binding to b2-AR when observed at 5, 10, 15, and 20 days under both cultural
conditions. Thyroid hormone caused an increase in binding of [125I]PIN to b2-AR
compared to thyroid hormone deficient controls at all ages of astrocyte culture. (3)
Saturation studies using [125I]PIN in astrocyte membranes prepared from 20-day-old
cultures showed a significant increase in the affinity of the receptors (KD) in the thyroid
hormone treated cells without any change in receptor number (Bmax). (4) b2-AR mRNA
levels were measured by real-time PCR during ontogenic development as well as during
exposure of 10-day-old hypothyroid cultures to normal levels of thyroid hormone for 2,
6, 12, and 24 h. None of the conditions caused any significant change in the b2-
adrenergic receptor mRNA levels when compared with corresponding hypothyroid
controls. (5) Over expression of b2-AR cDNA in hypothyroid astrocytes caused
morphological transformation in spite of the absence of thyroid hormone in the
medium. (6) Taken together, results suggest thyroid hormone causes a selective increase
in [125I]PIN binding to b2-AR due to increase in receptor affinity, which may lead to
maturation of astrocytes.
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